Are Natural Killer Cells Protecting the Metabolically Healthy Obese Patient?

Lynch, Lydia; O’Connell, Jean; Kwaśnik, Anna; Cawood, Thomas James; O’Farrelly, Cliona; O’Shea, Donal

doi:10.1038/oby.2008.565

Cited by 203 publications

(205 citation statements)

References 26 publications

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“…Determination of the prevalence of metabolically healthy obese individuals The diagnosis of MHO was obtained based on a BMIX30 kg/m 2 and six different sets of cardiometabolic abnormalities (Karelis et al, 2004;Meigs et al, 2006;AguilarSalinas et al, 2008;Wildman et al, 2008;Lynch et al, 2009), as described in a previous paper (Velho et al, 2010). As one definition of MHO includes CRP levels (Wildman et al, 2008), analysis of CRP levels was not performed for this definition.…”

Section: Biological Datamentioning

confidence: 99%

The association between inflammatory biomarkers and metabolically healthy obesity depends of the definition used

et al. 2011

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Background/Objectives: To assess the distribution of interleukin (IL)-1b, IL-6, tumour necrosis factor (TNF)-a and C-reactive protein (CRP) according to the different definitions of metabolically healthy obesity (MHO). Subjects/Methods: A total of 881 obese (body mass index (BMI) X30 kg/m 2 ) subjects derived from the population-based CoLaus Study participated in this study. MHO was defined using six sets of criteria including different combinations of waist, blood pressure, total high-density lipoprotein cholesterol or low-density lipoprotein -cholesterol, triglycerides, fasting glucose, homeostasis model, high-sensitivity CRP, and personal history of cardiovascular, respiratory or metabolic diseases. IL-1b, IL-6 and TNF-a were assessed by multiplexed flow cytometric assay. CRP was assessed by immunoassay. Results: On bivariate analysis some, but not all, definitions of MHO led to significantly lower levels of IL-6, TNF-a and CRP compared with non-MH obese subjects. Most of these differences became nonsignificant after multivariate analysis. An posteriori analysis showed a statistical power between 9 and 79%, depending on the inflammatory biomarker and MHO definition considered. Further increasing sample size to overweight þ obese individuals (BMIX25 kg/m 2 , n ¼ 2917) showed metabolically healthy status to be significantly associated with lower levels of CRP, while no association was found for IL-1b. Significantly lower IL-6 and TNF-a levels were also found with some but not all MHO definitions, the differences in IL-6 becoming nonsignificant after adjusting for abdominal obesity or percent body fat. Conclusions: MHO individuals present with decreased levels of CRP and, depending on MHO definition, also with decreased levels in IL-6 and TNF-a. Conversely, no association with IL-1b levels was found.

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Section: Biological Datamentioning

confidence: 99%

The association between inflammatory biomarkers and metabolically healthy obesity depends of the definition used

et al. 2011

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“…The diagnosis of MHO was obtained based on the joint combination of each obesity marker (BMI, waist circumference and body fat percentage) and six different sets of cardiometabolic abnormalities (Karelis et al, 2004;Meigs et al, 2006;Aguilar-Salinas et al, 2008;Wildman et al, 2008;Lynch et al, 2009) (Table 1). There were no exclusion criteria such as menopause, hormonal use and medications affecting metabolism, as well as diabetes and CVDs; participants were selected if they presented with overweight or obesity using the different anthropometric markers (BMI, waist or body fat).…”

Section: Determination Of the Prevalence Of Metabolically Healthy Obesementioning

confidence: 99%

“…There are currently no unique criteria for MHO, and several definitions have been proposed (Meigs et al, 2006;Aguilar-Salinas et al, 2008;Karelis, 2008;Wildman et al, 2008;Lynch et al, 2009). The criteria used to define MHO are summarized in Table 1.…”

Section: Introductionmentioning

confidence: 99%

Metabolically healthy obesity: different prevalences using different criteria

Velho

Paccaud

Waeber³

et al. 2010

Eur J Clin Nutr

217

185

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Objective: To estimate the prevalence of metabolically healthy obesity (MHO) according to different definitions. Methods: Population-based sample of 2803 women and 2557 men participated in the study. Metabolic abnormalities were defined using six sets of criteria, which included different combinations of the following: waist; blood pressure; total, high-density lipoprotein or low-density lipoprotein-cholesterol; triglycerides; fasting glucose; homeostasis model assessment; high-sensitivity C-reactive protein; personal history of cardiovascular, respiratory or metabolic diseases. For each set, prevalence of MHO was assessed for body mass index (BMI); waist or percent body fat. Results: Among obese (BMI X30 kg/m 2 ) participants, prevalence of MHO ranged between 3.3 and 32.1% in men and between 11.4 and 43.3% in women according to the criteria used. Using abdominal obesity, prevalence of MHO ranged between 5.7 and 36.7% (men) and 12.2 and 57.5% (women). Using percent body fat led to a prevalence of MHO ranging between 6.4 and 43.1% (men) and 12.0 and 55.5% (women). MHO participants had a lower odd of presenting a family history of type 2 diabetes. After multivariate adjustment, the odds of presenting with MHO decreased with increasing age, whereas no relationship was found with gender, alcohol consumption or tobacco smoking using most sets of criteria. Physical activity was positively related, whereas increased waist was negatively related with BMI-defined MHO. Conclusion: MHO prevalence varies considerably according to the criteria used, underscoring the need for a standard definition of this metabolic entity. Physical activity increases the likelihood of presenting with MHO, and MHO is associated with a lower prevalence of family history of type 2 diabetes.

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“…However as of yet, their role has not been fully elucidated in the chronic inflammation that is characteristic of obesity. Lynch et al have reported significant reductions of circulating NK cells in metabolically unhealthy obese subjects, suggesting that a lack of NK cells in the periphery is detrimental for metabolic health (83) . Lynch et al also reported significant expansions of circulating inhibitory-receptor bearing and CD69 + NK cells in metabolically unhealthy obese individuals, compared with healthy controls, suggesting that peripheral NK cells in metabolically unhealthy obese patients were activated but unable to elicit effector functions, making such individuals more susceptible to disease (83) .…”

Section: Natural Killer Cellsmentioning

confidence: 99%

“…CD8 + T Cytotoxicity -directly kill abnormal cells Promote inflammation (80) , macrophage recruitment (81,82) NK Cytotoxicity -kill abnormal cells Decreased in blood, impaired function (83) (89,90) iNKT, invariant natural killer T cells; MAIT, mucosal associated invariant T cells; NK, natural killer; VAT, visceral adipose tissue.…”

Section: M2mentioning

confidence: 99%

Obesity-associated cancer: an immunological perspective

et al. 2015

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Epidemiological studies have established an association between obesity, insulin resistance, type 2 diabetes and a number of cancer types. Research has focused predominantly on altered endocrine factors, growth factors and signalling pathways, with little known in man about the immune involvement in the relevant pathophysiological processes. Moreover, in an era of exciting new breakthroughs in cancer immunotherapy, there is also a need to study the safety and efficacy of immunotherapeutics in the complex setting of inflammatory-driven obesityassociated cancer. This review addresses key immune cell subsets underpinning obesityassociated inflammation and describes how such immune compartments might be targeted to prevent and treat obesity-associated cancer. We propose that the modulation, metabolism, migration and abundance of pro-and anti-inflammatory cells and tumour-specific T cells might be therapeutically altered to both restore immune balance, alleviating pathological inflammation, and to improve anti-tumour immune responses in obesity-associated cancer. Obesity: Cancer: Lymphocytes: Immunotherapeutics: InflammationThe burgeoning global health burden of obesity is of grave concern, affecting over half a billion adults worldwide, with approximately 3·5 million attributable deaths each year (1) . Despite national and international interventions to promote a healthy diet and lifestyle, recent reports predict that global obesity rates show no signs of abating, with predictions that half of all adults will be overweight or obese by 2030 (WHO). The worldwide prevalence of obesity almost doubled in the period 1980-2008. In 1980, 5 % of men and 8 % of women were obese and by 2008, these rates were 10 and 14 %, respectively. In many areas of the western world, the overweight phenotype is now the most prevalent body type. For example, in the USA in 2010 the prevalence of a BMI ≥ 25 was 69·2 %, with 35·9 % of people being obese (BMI ≥ 30) (2)

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Are Natural Killer Cells Protecting the Metabolically Healthy Obese Patient?

Cited by 203 publications

References 26 publications

The association between inflammatory biomarkers and metabolically healthy obesity depends of the definition used

The association between inflammatory biomarkers and metabolically healthy obesity depends of the definition used

Metabolically healthy obesity: different prevalences using different criteria

Obesity-associated cancer: an immunological perspective

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